Inhomogeneous mechanotransduction defines the spatial pattern of apoptosis-induced compensatory proliferation.


Journal

Developmental cell
ISSN: 1878-1551
Titre abrégé: Dev Cell
Pays: United States
ID NLM: 101120028

Informations de publication

Date de publication:
27 02 2023
Historique:
received: 20 09 2021
revised: 09 07 2022
accepted: 26 01 2023
pubmed: 22 2 2023
medline: 3 3 2023
entrez: 21 2 2023
Statut: ppublish

Résumé

The number of cells in tissues is controlled by cell division and cell death, and its misregulation could lead to pathological conditions such as cancer. To maintain the cell numbers, a cell-elimination process called apoptosis also stimulates the proliferation of neighboring cells. This mechanism, apoptosis-induced compensatory proliferation, was originally described more than 40 years ago. Although only a limited number of the neighboring cells need to divide to compensate for the apoptotic cell loss, the mechanisms that select cells to divide have remained elusive. Here, we found that spatial inhomogeneity in Yes-associated protein (YAP)-mediated mechanotransduction in neighboring tissues determines the inhomogeneity of compensatory proliferation in Madin-Darby canine kidney (MDCK) cells. Such inhomogeneity arises from the non-uniform distribution of nuclear size and the non-uniform pattern of mechanical force applied to neighboring cells. Our findings from a mechanical perspective provide additional insight into how tissues precisely maintain homeostasis.

Identifiants

pubmed: 36800994
pii: S1534-5807(23)00036-9
doi: 10.1016/j.devcel.2023.01.005
pmc: PMC7614677
mid: EMS177290
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

267-277.e5

Subventions

Organisme : European Research Council
ID : 101019835
Pays : International

Informations de copyright

Copyright © 2023 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests The authors declare no competing interests.

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Auteurs

Takumi Kawaue (T)

Mechanobiology Institute, National University of Singapore, Singapore; Institute for Integrated Cell-Material Sciences, Kyoto University, Kyoto, Japan.

Ivan Yow (I)

Mechanobiology Institute, National University of Singapore, Singapore.

Yuping Pan (Y)

Mechanobiology Institute, National University of Singapore, Singapore.

Anh Phuong Le (AP)

Mechanobiology Institute, National University of Singapore, Singapore.

Yuting Lou (Y)

Mechanobiology Institute, National University of Singapore, Singapore.

Mavis Loberas (M)

Mechanobiology Institute, National University of Singapore, Singapore.

Murat Shagirov (M)

Mechanobiology Institute, National University of Singapore, Singapore.

Xiang Teng (X)

Mechanobiology Institute, National University of Singapore, Singapore.

Jacques Prost (J)

Physico Chimie Curie, Institut Curie, CNRS, UMR 168, 75005 Paris, France.

Tetsuya Hiraiwa (T)

Mechanobiology Institute, National University of Singapore, Singapore.

Benoit Ladoux (B)

Université Paris Cité, CNRS, Institut Jacques Monod, F-75013 Paris, France.

Yusuke Toyama (Y)

Mechanobiology Institute, National University of Singapore, Singapore; Department of Biological Sciences, National University of Singapore, Singapore. Electronic address: dbsty@nus.edu.sg.

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